Introduction: Chronic tophaceous gout is a rare cause of parathyroid hormone (PTH)-independent hypercalcemia. This is due to increased 1-alpha hydroxylase activity within granulomatous inflammation surrounding gouty tophi, resulting in excess calcitriol production. In advanced disease, immobilization from pain and joint deformity may further exacerbate hypercalcemia due to immobilizationrelated bone resorption, leading to clinically significant symptoms and complications. Case: A 59-year-old male with chronic tophaceous gout complicated with CKD and nephrocalcinosis was referred for inpatient evaluation of hypercalcemia. He had an episode of acute pancreatitis attributed to hypercalcemia 1 month prior. Serum calcium levels have risen progressively over the preceding year, from 2.48 mmol/L (reference 2.0–2.65) to 3.17 mmol/L. His gout was poorly controlled with uric acid levels ranging 641–709 umol/L, with extensive tophi over the upper and lower limbs and gluteal regions. He had been maintained on low-dose allopurinol 150 mg/day for 2 years. Functionally, he was largely bedbound and wheelchair-dependent. On admission, corrected calcium was 3.48 mmol/L with suppressed intact parathyroid hormone (<0.6 pmol/L) consistent with PTH-independent hypercalcemia. Malignancy and myeloma workup, including tumor markers, was unremarkable. Serum phosphate (0.9 mmol/L) and alkaline phosphatase (152 IU/L) were normal. Hypercalcemia persisted despite intravenous hydration and calcitonin. Low-dose prednisolone was then initiated, followed by pamidronate, resulting in normalization of corrected calcium to 2.17 mmol/L. He remained normocalcemic while on tapering prednisolone for a month. However, calcium rebounded months after cessation. Gradual escalation of allopurinol to 900 mg/day improves uric acid levels to 389–429 umol/L with better functional status (standing unsupported briefly and mobilizing with assistance). However, calcium remains moderately elevated 2.65–2.85 mmol/L. Conclusion This case highlights severe tophaceous gout as a rare but significant cause of PTH-independent hypercalcemia, in which glucocorticoids can be effective in treating refractory hypercalcemia. It also underscores the importance of addressing the underlying disease through optimization of urate-lowering therapy and functional rehabilitation.

Introduction: Rheumatoid arthritis (RA) is an autoimmune systemic inflammatory disorder characterised by symmetrical polyarthritis which leads to damage of joints if untreated. Early diagnosis and treatment of RA to achieve tight control of the disease will improve outcome and prevent disability. Objective: We aimed to examine the delays in the diagnosis of RA in patients presenting to the Rheumatology Unit, Sarawak General Hospital (SGH). Methods: Data on demographics and various delays were collected from the medical records from January 2015 until March 2018. Patient delay is defined as from the time onset of symptom to the first primary care presentation. Primary care delay is defined as from the first primary care presentation to referral to rheumatology. Rheumatology delay is defined as from rheumatology referral to appointment at the rheumatology clinic. Disease modifying anti-rheumatic drugs (DMARDS) delay is defined as from the rheumatology clinic appointment to starting DMARDS. Total delay is from symptom onset to starting DMARDS. Results: There were 84 new patients diagnosed with rheumatoid arthritis, out of which 66 were females (78.6%). The mean age was 54.1±12.0 years. Only 19 patients (22.6%) were treated with DMARDS within 12 weeks of symptom onset. The median time for patient delay was four weeks (Interquartile range (IQR) 2-20 weeks), while the median time primary care delay was 11 weeks (IQR 4-24 weeks). The median time for rheumatology delay was zero weeks (IQR 0- 1 week) and the DMARDS delay was zero week (IQR 0). The median time from symptom onset to DMARDS initiation was 23.5 weeks (IQR 13.25-51 weeks). Conclusion: The delays in the diagnosis of rheumatoid arthritis were mainly from the patient and primary care.